Evidence map›Paper›PMID 24273177›Full record

ArticleThe Journal of infectious diseases2014

The complement C3a receptor is critical in defense against Chlamydia psittaci in mouse lung infection and required for antibody and optimal T cell response.

Pavel Dutow, Beate Fehlhaber, Jenny Bode, Robert Laudeley, Claudia Rheinheimer, Silke Glage, Rick A Wetsel, Oliver Pabst, Andreas Klos

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.8field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Review
  3. Vaccines · 2021
    Article
  4. Article
  5. Complement andFrontiers in immunology · 2021
    Article
  6. Complement andFrontiers in immunology · 2021
    Article
  7. Article
  8. Article
  9. An Ancient Molecular Arms Race:Frontiers in immunology · 2020
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 3 countries.

Pavel DutowInstitute of Medical Microbiology and Hospital Epidemiology, Hannover Medical School (MHH).
Beate Fehlhaber
Jenny Bode
Robert Laudeley
Claudia Rheinheimer
Silke Glage
Rick A Wetsel
Oliver Pabst
Andreas Klos
Medizinische Hochschule Hannover · DEInstitute of Medical Microbiology and Hygiene · DEBrown Foundation · USInstitute of Laboratory Animal Science · CN

Funding

MURINE COMPLEMENT C5 DEFICIENCY--MOLECULAR BASISR01AI025011 · NIAID · WASHINGTON UNIVERSITY · PI WETSEL, RICK A. · 1987 to 2017
$4.6M
NIAID NIH HHS R01 AI025011
6 · The paper itself

Abstract

backgroundThe complement system protects against extracellular pathogens and links innate and adaptive immunity. In this study, we investigated the anaphylatoxin C3a receptor (C3aR) in Chlamydia psittaci lung infection and elucidated C3a-dependent adaptive immune mechanisms.

methodsSurvival, body weight, and clinical score were monitored in primary mouse infection and after serum transfer. Bacterial load, histology, cellular distribution, cytokines, antibodies, and lymphocytes were analyzed.

resultsC3aR(-/-) mice showed prolonged pneumonia with decreased survival, lower weight, and higher clinical score. Compared to wild-type mice bacterial clearance was impaired, and inflammatory parameters were increased. In lung-draining lymph nodes of C3aR(-/-) mice the total number of B cells, CD4(+) T cells, and Chlamydia-specific IFN-γ(+) (CD4(+) or CD8(+)) cells was reduced upon infection, and the mice were incapable of Chlamydia-specific immunoglobulin M or immunoglobulin G production. Performed before infection, transfer of hyperimmune serum prolonged survival of C3aR(-/-) mice.

conclusionsC3a and its receptor are critical for defense against C. psittaci in mouse lung infection. In this model, C3a acts via its receptor as immune modulator. Enhancement of specific B and T cell responses upon infection with an intracellular bacterium were identified as hitherto unknown features of C3a/C3aR. These new functions might be of general immunological importance.

Indexed as

Adaptive ImmunityAnimalsAntibodies, BacterialChlamydophila InfectionsChlamydophila psittaciImmunoglobulin GImmunoglobulin MLungMaleMicePneumonia, BacterialReceptors, ComplementT-LymphocytesAntibodies, Bacterialcomplement C3a receptorImmunoglobulin GImmunoglobulin MReceptors, Complementadaptive immunityanaphylatoxinbacteriumC3a receptorchlamydiaChlamydia psittacicomplementdefenseintracellular

Identifiers

PMID24273177
PMCPMC3969542
OpenAlexW2113183663

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.